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The Role of Leptin in the Development of the Cerebral Cortex in Mouse Embryos

Department of Developmental Biology (J.U., R.H., T.H., Y.K., H.O.), Faculty of Medicine, Shimane University, Izumo 693-8501, Japan; Department of Oral and Maxillofacial Surgery (H.S.), Kobe University Graduate School of Medicine, Kobe 650-0017, Japan; Central Institute for Experimental Animals (Y.S., K.H., T.N.), Kawasaki 216-0001, Japan; Department of Food Science (Y.K.), Shimane Women’s College, Matsue 690-0044, Japan; and Department of Genome Sciences (Y.M.), Faculty of Medical Sciences, Kobe University, Graduate School of Medicine, Kobe 650-0017, Japan

Address all correspondence and requests for reprints to: Jun Udagawa, Department of Developmental Biology, Faculty of Medicine, Shimane University, Izumo 693-8501, Japan. E-mail: jun{at}med.shimane-u.ac.jp.

Leptin is detected in the sera, and leptin receptors are expressed in the cerebrum of mouse embryos, suggesting that leptin plays a role in cerebral development. Compared with the wild type, leptin-deficient (ob/ob) mice had fewer cells at embryonic day (E) 16 and E18 and had fewer 5-bromo-2'-deoxyuridine⁺ cells at E14 and E16 in the neuroepithelium. Intracerebroventricular leptin injection in E14 ob/ob embryos increased the number of neuroepithelium cells at E16. In cultured neurosphere cells, leptin treatment increased Hes1 mRNA expression and maintained neural progenitors. Astrocyte differentiation was induced by low-dose (0.1 µg/ml) but not high-dose (1 µg/ml) leptin. High-dose leptin decreased Id mRNA and increased Ngn1 mRNA in neurosphere cells. The neuropeptide Y mRNA level in the cortical plate was lower in ob/ob than the wild type at E16 and E18. These results suggest that leptin maintains neural progenitors and is related to glial and neuronal development in embryos.

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